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| title | chunk | source | category | tags | date_saved | instance |
|---|---|---|---|---|---|---|
| Abortion–breast cancer hypothesis | 2/4 | https://en.wikipedia.org/wiki/Abortion–breast_cancer_hypothesis | reference | science, encyclopedia | 2026-05-05T09:15:13.301340+00:00 | kb-cron |
In early pregnancy, levels of estrogen, progesterone, and estradiol increase, leading to breast growth in preparation for lactation. Proponents speculate that if this process is interrupted by an abortion or miscarriage—before full maturity (differentiation) in the third trimester—then more immature cells could be left than there were prior to the pregnancy. These immature cells could then be exposed to carcinogens and hormones over time, resulting in a greater potential risk of breast cancer. This mechanism was first proposed and explored in rat studies conducted in the 1980s. Breast tissue contains many lobes (segments) and these contain lobules which are groups of breast cells. There are four types of lobules:
Type 1 has 11 ductules (immature) Type 2 has 47 ductules (immature) Type 3 has 80 ductules (mature, fewer hormone receptors) Type 4 are fully matured (cancer resistant) and contain breast milk During early pregnancy, type 1 lobules quickly become type 2 lobules because of changes in estrogen and progesterone levels. Maturing into type 3 and then reaching full differentiation as type 4 lobules requires an increase of human placental lactogen (hPL) which occurs in the last few months of pregnancy. According to the abortion–breast cancer hypothesis, if an abortion were to interrupt this sequence then it could leave a higher ratio of type 2 lobules than existed prior to the pregnancy. Russo and Russo have shown that mature breast cells have more time for DNA repair with longer cell cycles, accounting for the slightly reduced risk of breast cancer for parous women against the baseline risk for women who have never conceived and those who have conceived and terminated their pregnancies. Later on, Russo et al. found that placental human chorionic gonadotropin (hCG) induces the synthesis of inhibin by the mammary epithelium. Bernstein et al. independently observed a reduced breast cancer risk when women were injected with hCG for weight loss or infertility treatment. Contrary to the ABC hypothesis, Michaels et al. hypothesize since hCG plays a role in cellular differentiation and may activate apoptosis, as levels of hCG increase early on in human pregnancy, "an incomplete pregnancy of short duration might impart the benefits of a full-term pregnancy and thus reduce the risk of breast cancer."
== History == The first study involving statistics on abortion and breast cancer was a broad study in 1957 examining common cancers in Japan. The researchers were cautious about drawing any conclusions from their unreliable methodologies. During the 1960s several studies by Brian MacMahon et al. in Europe and Asia touched on a correlation between abortion and breast cancer. Their 1973 paper published in the Journal of the National Cancer Institute inaccurately concluded that "where a relationship was observed, abortion was associated with increased, not decreased, risk." Research relevant to the current ABC discussion focuses on more recent large cohort studies, a few meta-analyses, many case-control studies, and several early experiments with rats.
=== Rat models === Russo & Russo from the Fox Chase Cancer Center in Philadelphia conducted a study in 1980 examining the proposed correlation between abortion and breast cancer. While analysing the effects of the carcinogen 7,12-Dimethylbenz(a)anthracene (DMBA) on the DNA labeling index (DNA-LI) in terminal end buds (TEBs), terminal ducts (TDs) and alveolar buds (ABs) of Sprague-Dawley rats in various stages of reproductive development, they found that rats who had interrupted pregnancies had no noticeable increase in risk for cancer. However, they did find that pregnancy and lactation provided a protective measure against various forms of benign lesions, such as hyperplastic alveolar nodules and cysts. While results did suggest that rats who had interrupted pregnancies might be subject to "similar or even higher incidence of benign lesions" than virgin rats, there was no evidence to suggest that abortion would result in a higher incidence of carcinogenesis. A more thorough examination of the phenomenon was conducted in 1982, confirming the results. A later study in 1987 further explained their previous findings. After differentiation of the mammary gland resulting from a full-term pregnancy of the rat, the rate of cell division decreases and the cell cycle length increases, allowing more time for DNA repair. Despite the fact that the Russos' studies found similar risk rates between virgin and pregnancy interrupted rats, their research would be used to support the contention that abortion created a greater risk of breast cancer for the next twenty years. However, because rats do not exhibit naturally occurring breast cancer, the extrapolation of these results to human abortion and breast cancer is viewed as dubious.